UMLS:C0018099 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Niacin has been used for many years to treat hyperlipidemia. It has been shown to reduce coronary death and non-fatal myocardial infarction and, in a separate analysis of long-term (15-year) follow-up, all cause mortality. It reduces total cholesterol, low density lipoprotein cholesterol (LDL-C) and triglycerides and increases high density lipoprotein cholesterol (HDL-C). Sustained-release niacin may be associated with more dramatic changes in LDL-C and triglyceride, whereas the short acting preparation causes greater increases in HDL-C. The increase of HDL-C occurs at a lower dose (1500 mg/day) than the reduction of LDL-C (> 1500 mg/day). Niacin also favorably influences other lipid parameters including lipoprotein(a) [Lp(a)], alimentary lipemia, familial defective apolipoprotein B-100 and small dense LDL. Combination of niacin with a bile acid sequestrant or a reductase inhibitor represents a powerful lipid-altering regimen. Whereas the reductase inhibitors and bile acid binding resins primarily affect LDL-C, the combined therapy has a synergistic effect to reduce LDL-C and, in addition, the niacin reduces triglycerides and increases HDL-C. The major drawback in the use of niacin is associated side effects (flushing and palpitations) and toxicity (worsening of diabetes control, exacerbation of peptic ulcer disease, gout, hepatitis). Niacin has a long history of use as a lipid lowering agent and has several attractive features. Unfortunately, the side effect profile of this agent warrants its use only in patients with marked dyslipidemia in whom side effects and potential toxicity are closely monitored.
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PMID:New developments in the use of niacin for treatment of hyperlipidemia: new considerations in the use of an old drug. 885 85

Diuretics were used in most of the major trials that demonstrated that lowering the blood pressure reduced cardiovascular morbidity and mortality. Nevertheless in the second half of the eighties, there were misgivings about the widespread use of thiazide diuretics, driven in part by the relative failure of the large trials to reduce myocardial infarction-to the extent predicted by large scale epidemiological studies. There was much attention on metabolic side effects of thiazide diuretics including dyslipidaemia, glucose intolerance, hypokalaemia, hyperuricaemia, and then microalbuminuria particularly in diabetic subjects. These issues were current when JNC (IV) (1988) and the WHO-ISH guidelines (1989) were being written. Three major clinical trials SHEP, STOP and MRC published in the early nineties established that thiazide diuretics alone, or in combination with beta blockers, did reduce cardiovascular morbidity and mortality in elderly subjects with hypertension. All guidelines published since 1993 include diuretics among the first line drugs. Possibly the most important factor in the restoration of diuretics has been the use of progressively lower doses that minimise the metabolic side effects. Diuretics are effective as monotherapy in the treatment of mild essential hypertension and of isolated systolic hypertension in elderly subjects. They are very useful in combination with beta blockers or with ACE inhibitors. They should be avoided in patients with gout and should not be used as first line drugs in patients with diabetes. They should only be used with caution in young obese subjects with dyslipidaemia and increased risk of coronary artery disease, facing many decades of treatment for hypertension. However there is no doubt that diuretics are effective, cheap and have a central role in the control of hypertension in all communities around the world.
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PMID:[Role of diuretics in the treatment of hypertension: from large controlled trials to international guidelines]. 895 12

The objective of the study was to determine if male subjects with coronary atherosclerotic heart disease (CHD) without major CHD risk factors have hyperinsulinemia and related metabolic changes. Previous studies suggested that hyperinsulinemia is a CHD risk factor, but they did not entirely exclude concurrent metabolic abnormalities. A prospective, comparative, cross-sectional study in a tertiary care teaching hospital in Mexico City was conducted in 15 men who had suffered myocardial infarction 6 to 24 months before and had significant coronary occlusion on angiography. Control group was formed by 15 age-matched healthy men. None had hypertension, obesity, diabetes, gout, glucose intolerance or hyperlipidemia. Body mass index (BMI), waist/hip ratio (WHR), blood pressure (BP); oral glucose tolerance test (OGTT) with measurement of serum glucose, insulin and C-peptide every 30 min for 2 h, fasting serum cholesterol, triglycerides and uric acid, areas under curve (AUC) of glucose and insulin, insulin/glucose ratio and insulin sensitivity index were calculated. BMI, WHR and BP were similar in both groups. Fasting and post-load serum glucose and insulin concentrations were significantly higher in CHD than in control group (p < 0.01); fasting glucose 5.9 +/- 0.6 vs. 4.8 +/- 0.7 nmol/1, 2-h glucose 8.3 +/- 0.6 vs. 7.3 +/- 0.9 mmol/l, fasting insulin 17.5 +/- 1.2 vs. 15.3 +/- 1.7 pmol/l, 2 h insulin 448 +/- 108 vs. 282 +/- 87 pmol/l in CHD and control group, respectively. AUC of glucose, AUC of insulin, insulin/glucose ratio, post load C-peptide, serum cholesterol, triglycerides and uric acid levels were also significantly higher in CHD than in healthy controls. Insulin sensitivity index was significantly lower in patients with CHD (27.7 +/- 8.3) than in healthy control subjects (73.9 +/- 18) (p < 0.001). Patients with CHD have hyperinsulinemia and subtle metabolic abnormalities related with insulin resistance even in absence of overt risk factors.
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PMID:Hyperinsulinemia in patients with coronary heart disease in absence of overt risk factors. 907 98

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation. The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status. During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.
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PMID:Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University. 1207 15

Serum uric acid (UA) has been implicated in the pathogenesis of hypertension. We investigated the relationship of serum UA to hypertension incidence and blood pressure (BP) progression in 3329 Framingham Study participants (mean age 48.7 years; 55.6% women) free of hypertension, myocardial infarction, heart failure, renal failure, or gout. At follow-up 4 years from baseline, 458 persons (13.8%) had developed hypertension, and 1201 persons (36.1%) had experienced progression to a higher BP stage. Age- and sex-adjusted rates of hypertension incidence increased progressively from 9.8% for the lowest quartile to 15.6% for the top quartile of serum UA; BP progression rates increased from 32.8% (lowest quartile) to 39.6% (top quartile). In multivariable analyses adjusting for age, sex, body mass index, diabetes, smoking, alcohol intake, serum creatinine, proteinuria, glomerular filtration rate, baseline BP, and interim weight change, a 1 SD higher serum UA was associated with an odds ratio (OR) of 1.17 (95% confidence interval [CI], 1.02 to 1.33) for developing hypertension, and an OR of 1.11 (95% CI, 1.01 to 1.23) for BP progression. In analyses of a subsample of 3157 individuals not on antihypertensive treatment at the follow-up examination, serum UA was positively associated with changes in systolic (P=0.02) and diastolic pressure 4 years later (P=0.04). In summary, serum UA level was an independent predictor of hypertension incidence and longitudinal BP progression at short-term follow-up in our community-based sample.
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PMID:Relations of serum uric acid to longitudinal blood pressure tracking and hypertension incidence. 1555 87

The association of elevated serum uric acid (hyperuricemia, gout) with the presence of classical coronary risk factors and coronary artery disease or myocardial infarction has been analysed in many epidemiological studies. In this paper the urid acid metabolism, the factors influancing on this metabolism, the laboratory hyperurycemia criteria and the mode of hyperuricemia treatment are presented. The hyperuricemia and it's collaboration with the other coronary risk factors are analysed as an independent risk factors. Hyperuricemia is described as an increased concentration of uric acid in blood. The urate concentration is elevated when the upper level of arbitrary accepted value is exceeded. That corresponds to the mean value of urate concentration of particular sex and age plus two standard deviations. In most cases of epidemiologic investigations the upper normal range of concentration equals 6 mg/dl for women and 7 mg/dl for men. An increased level of uric acid leads to urate gout (diathesis urica). An increased level of urate in serum is connected with numerous cardiovascular risk factors such as: arterial hypertension, hyperglycemia, diabetes and male sex. But up today, hyperuricemia is not used as independent direct risk factor, so the reduction of uric acid is not obligatory recommended in guidelines for prevention of cardiovascular diseases and stroke.
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PMID:[Hyperuricemia]. 1649 14

To examine whether serum urate level and other aspects of gouty arthritis are independently associated with Q-wave myocardial infarction (QWMI) in gouty population, we performed a cross-sectional study. A total of 22,572 gouty cases were enrolled. QWMI was defined as a positive finding by resting electrocardiographic criteria excluding the conditions producing pseudoinfarction. The variables of gout were tested univariately and multivariately, controlling for the covariates by logistic regression analysis. The above analysis was then repeated in subgroups of young-aged (<50 years), old-aged (> or = 50 years), male, and female patients. Increased serum urate level was significantly associated with QWMI in all subjects and male subgroup [odds ratio (OR), 1.120; 95% confidence interval (CI), 1.020-1.229; OR, 1.106; 95% CI, 1.001-1.223, respectively, for each mg/dl increment]. After controlling for serum urate level and the covariates, increased affected joint count was also independently associated with QWMI finding in all subjects, male and old-aged subgroups (OR, 1.098; 95% CI, 1.014-1.189; OR, 1.094; 95% CI, 1.005-1.192; OR, 1.095; 95% CI, 1.001-1.199, respectively). Tophi formation was independently associated with QWMI in young-aged subgroup (OR, 2.494; 95% CI, 1.159-5.366). None of the variables of gout including hyperuricemia was significantly associated with QWMI in female subgroup after controlling for covariates. This study first demonstrates that gout is associated with QWMI by both the severity of gouty arthritis and serum urate level, while the association of urate to QWMI could be different between age strata and genders.
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PMID:Severity of gouty arthritis is associated with Q-wave myocardial infarction: a large-scale, cross-sectional study. 1668 95

The association of elevated serum uric acid (hyperuricemia, gout) with the presence of classical coronary risk factors and coronary artery disease (CAD) or myocardial infarction (MI) has been analysed in many epidemiological studies. Numerous studies have revealed that hypertension, high body mass index (BMI), lipid disorders (especially raised triglycerides--TG level and low high dense lipoprotein cholesterol HDL-C level), increased creatinine or insulin levels have caused hyperuricemia. No association has been observed between hyperuricemia and diabetes type 2 and uricemia and glicemia. But in some studies the relationship between cholesterol and uric acid levels has been not confirmed. Hyperuricemia has been observed in patients with non-treated hypertension. Gout has often occurred with typical disorders for the metabolic syndrome X. Significant correlation of the serum uric level and the CAD presence and severity of coronary atherosclerosis confirmed by coronary angiography has been observed in women. Hyperuricemia has also indirect influence on progress of CAD by physical activity restriction, what causes sedentary mode of life and lead to obesity. Obesity is a known risk factor diabetes, lipid disorders and hypertension. To recapitulate, it is a matter of controversy as to whether uric acid is an independent cardiovascular risk factor or rather it only represents reinforcement of typical risk factor.
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PMID:[Is hyperuricemia a cardiovascular risk factor?]. 1701 83

Antihypertensive therapy has been associated with 35 to 40% reduction in stroke incidence and 20 to 25% reduction in myocardial infarction. Antihypertensive drugs have various metabolic and endocrine activities. Their effect on electrolytes and hormones which modify the serum levels of electrolytes (such as aldosterone, angiotensine II and brain natriuretic peptide) is reviewed. Antihypertensive drugs may also modify risk factors for cardiovascular disease such as cholesterol, CRP hs, as well as urate acid and insulin resistance. Diuretics and betablockers increase this resistance whereas, it is decreased by certain enzyme conversion inhibitors and certain angiotensine II receptor blockers, partially through adiponectin release. Endocrine side effects of antihypertensive drugs such as weight gain, diabetes, gout, osteoporosis, impotence are discussed. They may decrease adherence to medication. Therefore we recommend if possible a low dose combination of antihypertensive drugs.
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PMID:[Metabolic and endocrine effects of antihypertensive drugs]. 1744 3

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